Abstract

Insomnia and depression are highly co-morbid conditions that share a complex, bi-directional relationship. By reviewing the literature examining the links between insomnia and depression, it becomes apparent that insomnia symptoms need to be directly targeted alongside depression symptoms when co-morbidities exist for optimal outcomes. The most common treatment in Australia for co-morbid insomnia and depression is currently antidepressant medication. Because a large percentage of individuals given antidepressants fail to remit from their depression and insomnia symptoms, an effective adjunct treatment to antidepressants for co-morbid insomnia and depression is required. Cognitive behavioural therapy for insomnia (CBT-I) is an empirically validated treatment for insomnia, and is efficacious in improving insomnia that is co-morbid with depression. Recent evidence also suggests that CBT-I produces significant improvements in depression severity. The main aim of the thesis was therefore to develop a cost-effective CBT-I intervention that could be easily administered, distributed and implemented on a wide-scale basis, both on its own for insomnia, and primarily as an adjunct therapy for co-morbid insomnia and depression. A therapist manual of CBT-I, based on the latest empirical findings, was specifically developed to increase consistency and ease of treatment administration by therapists wanting to deliver CBT-I treatment. A resource booklet was also developed to give to all individuals undergoing CBT-I treatment, to ensure that they were provided with the latest information about sleep and how to reduce their insomnia severity. A randomised controlled trial was then developed to investigate the efficacy of this CBT-I intervention in individuals with co-morbid insomnia and depression whose symptoms have failed to remit through antidepressant treatment. Forty-one participants (aged 18-64 years) were randomized to receive four sessions of either CBT-I or sleep education (self-help therapy) over an 8-week period (one session every two weeks). Participants had been treated with antidepressants for at least six weeks prior to screening, but were otherwise healthy. The Insomnia Severity Index and the Beck Depression Inventory were assessed at baseline, following each session, and at 3-month follow-up. Secondary outcomes were sleep quality and duration (actigraphy and self-report), anxiety, fatigue, and daytime sleepiness. Results indicated that CBT-I, compared to sleep education, produced significantly reduced depression and insomnia severity, and improved anxiety, fatigue, sleep quality and sleep efficiency. It is the first randomised controlled trial of CBT-I for co-morbid insomnia and depression, with an active control treatment, to show significant reductions in both insomnia and depression severity at post-treatment and follow-up. Large effect sizes were found for both insomnia and depression at post-treatment, and these effect sizes increased further by three month follow-up. At follow-up, ten times more CBT-I participants were in remission from both insomnia and depression than sleep education participants. This demonstrates that CBT-I is an efficacious treatment for co-morbid insomnia and depression, and should be considered an important adjunct therapy in individuals whose symptoms have not remitted through antidepressant treatment. Following the positive results of the randomised controlled trial, the proposed mediators of CBT-I were examined to determine which aspects of the intervention had the largest influence on reductions in insomnia and depression severity at post-treatment and 3-month follow-up. Changes in time-in-bed, bedtime variability, rise-time variability, sleep hygiene practices, dysfunctional beliefs about sleep and stress levels were assessed as potential mediators. Post-treatment results indicated that the significantly reduced depression severity through CBT-I was primarily via reduced stress levels, improved sleep hygiene practices, and other therapeutic effects of CBT-I, whereas reduced insomnia severity was primarily via reduced dysfunctional beliefs about sleep. By follow-up, the significantly reduced depression severity in the CBT-I group was primarily via reduced stress levels and reduced dysfunctional beliefs about sleep, whereas reduced dysfunctional beliefs about sleep and other therapeutic effects of CBT-I explained the significantly reduced insomnia severity. These results indicate that reducing stress levels through CBT-I treatment is required for optimal depression outcomes, whereas reducing dysfunctional beliefs about sleep is essential for optimal insomnia outcomes. Improving sleeping practices behaviourally is important for initial depression improvements, but reducing dysfunctional beliefs about sleep becomes more important for longer-term remission of depression symptoms. Other non-factual therapeutic elements of CBT-I treatment appear to be important, and may lead to a greater willingness to engage in the CBT-I strategies, which can improve depression in the short-term and insomnia in the longer-term. These mediators of CBT-I treatment had not been specifically examined in individuals with co-morbid insomnia and depression before this study. Their identification suggests that relaxation and behavioural sleep interventions should be prioritized initially through CBT-I for co-morbid insomnia and depression, followed by cognitive interventions to target unhelpful beliefs about sleep. By increasing the efficiency of CBT-I, optimal treatment outcomes can be achieved for individuals with co-morbid insomnia and depression, and the risk of future relapse can be minimized.

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